Controlling the chromatin organization of vitamin D target genes by multiple vitamin D receptor binding sites

2007 ◽  
Vol 103 (3-5) ◽  
pp. 338-343 ◽  
Author(s):  
Carsten Carlberg ◽  
Thomas W. Dunlop ◽  
Anna Saramäki ◽  
Lasse Sinkkonen ◽  
Merja Matilainen ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Receptor Binding ◽  
Binding Sites ◽  
Target Genes ◽  
Chromatin Organization

scholarly journals Characterization of Genomic Vitamin D Receptor Binding Sites through Chromatin Looping and Opening

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e96184 ◽  
Author(s):  
Sabine Seuter ◽  
Antonio Neme ◽  
Carsten Carlberg
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Receptor Binding ◽  
Binding Sites ◽  
Chromatin Looping

scholarly journals The Number of Vitamin D Receptor Binding Sites Defines the Different Vitamin D Responsiveness of theCYP24Gene in Malignant and Normal Mammary Cells

2010 ◽  
Vol 285 (31) ◽  
pp. 24174-24183 ◽  
Author(s):  
Juha M. Matilainen ◽  
Marjo Malinen ◽  
Mikko M. Turunen ◽  
Carsten Carlberg ◽  
Sami Väisänen
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Receptor Binding ◽  
Binding Sites ◽  
Mammary Cells

scholarly journals Nutraceuticals Derived From Pomegranate Selectively Enhance Vitamin D Receptor Signaling to Amplify Key Vitamin D Target Genes

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Sarah Livingston ◽  
Daniel Lucas ◽  
Marya S. Sabir ◽  
Sanchita Mallick ◽  
Hespera Purdin ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Target Genes ◽  
Receptor Signaling

scholarly journals Genome-wide effects of chromatin on vitamin D signaling

2020 ◽  
Vol 64 (4) ◽  
pp. R45-R56 ◽  
Author(s):  
Andrea Hanel ◽  
Henna-Riikka Malmberg ◽  
Carsten Carlberg
Keyword(s):  
Vitamin D ◽  
Binding Sites ◽  
Target Genes ◽  
Chromatin Accessibility ◽  
Transcription Start Sites ◽  
Dihydroxyvitamin D ◽  
Genome Wide ◽  
Spatio Temporal ◽  
Vitamin D Signaling ◽  
The Impact

Molecular endocrinology of vitamin D is based on the activation of the transcription factor vitamin D receptor (VDR) by the vitamin D metabolite 1α,25-dihydroxyvitamin D3. This nuclear vitamin D-sensing process causes epigenome-wide effects, such as changes in chromatin accessibility as well as in the contact of VDR and its supporting pioneer factors with thousands of genomic binding sites, referred to as vitamin D response elements. VDR binding enhancer regions loop to transcription start sites of hundreds of vitamin D target genes resulting in changes of their expression. Thus, vitamin D signaling is based on epigenome- and transcriptome-wide shifts in VDR-expressing tissues. Monocytes are the most responsive cell type of the immune system and serve as a paradigm for uncovering the chromatin model of vitamin D signaling. In this review, an alternative approach for selecting vitamin D target genes is presented, which are most relevant for understanding the impact of vitamin D endocrinology on innate immunity. Different scenarios of the regulation of primary upregulated vitamin D target genes are presented, in which vitamin D-driven super-enhancers comprise a cluster of persistent (constant) and/or inducible (transient) VDR-binding sites. In conclusion, the spatio-temporal VDR binding in the context of chromatin is most critical for the regulation of vitamin D target genes.

Functional characterization of WT1 binding sites within the human vitamin D receptor gene promoter

2001 ◽  
Vol 7 (2) ◽  
pp. 187-200 ◽  
Author(s):  
TAE HO LEE ◽  
JERRY PELLETIER
Keyword(s):  
Gene Expression ◽  
Vitamin D ◽  
Transcription Factor ◽  
Vitamin D Receptor ◽  
Binding Sites ◽  
Wilms Tumor ◽  
Cdna Array ◽  
Transcriptional Level ◽  
Vdr Gene ◽  
Downstream Target

The Wilms’ tumor suppressor gene, wt1, encodes a zinc finger transcription factor that can regulate gene expression. It plays an essential role in tumorigenesis, kidney differentiation, and urogenital development. To identify WT1 downstream targets, gene expression profiling was conducted using a cDNA array hybridization approach. We confirm herein that the human vitamin D receptor (VDR), a ligand-activated transcription factor, is a WT1 downstream target. Nuclear run on experiments demonstrated that the effect of WT1 on VDR expression is at the transcriptional level. Transient transfection assays, deletion mutagenesis, electrophoretic mobility shift assays, and chromatin immunoprecipitation assays suggest that, although WT1 is presented with a possibility of three binding sites within the VDR promoter, activation of the human VDR gene appears to occur through a single site. This site differs from a previously identified WT1-responsive site in the murine VDR promoter (Maurer U, Jehan F, Englert C, Hübinger G, Weidmann E, DeLucas HF, and Bergmann L. J Biol Chem 276: 3727–3732, 2001). We also show that the products of a Denys-Drash syndrome allele of wt1 inhibit WT1-mediated transactivation of the human VDR promoter. Our results indicate that the human VDR gene is a downstream target of WT1 and may be regulated differently than its murine counterpart.

Molecular network of chromatin immunoprecipitation followed by deep sequencing-based vitamin D receptor target genes

2013 ◽  
Vol 19 (8) ◽  
pp. 1035-1045 ◽  
Author(s):  
Jun-ichi Satoh ◽  
Hiroko Tabunoki
Keyword(s):  
Multiple Sclerosis ◽  
Vitamin D ◽  
Vitamin D Receptor ◽  
Deep Sequencing ◽  
Immune Cells ◽  
Chromatin Immunoprecipitation ◽  
Target Genes ◽  
Molecular Network ◽  
Genome Wide

Background: Vitamin D is a liposoluble vitamin essential for calcium metabolism. The ligand-bound vitamin D receptor (VDR), heterodimerized with retinoid X receptor, interacts with vitamin D response elements (VDREs) to regulate gene expression. Vitamin D deficiency due to insufficient sunlight exposure confers an increased risk for multiple sclerosis (MS). Objective: To study a protective role of vitamin D in multiple sclerosis (MS), it is important to characterize the global molecular network of VDR target genes (VDRTGs) in immune cells. Methods: We identified genome-wide VDRTGs collectively from two distinct chromatin immunoprecipitation followed by deep sequencing (ChIP-Seq) datasets of VDR-binding sites derived from calcitriol-treated human cells of B cell and monocyte origins. We mapped short reads of next generation sequencing (NGS) data on hg19 with Bowtie, detected the peaks with Model-based Analysis of ChIP-Seq (MACS), and identified genomic locations by GenomeJack, a novel genome viewer for NGS platforms. Results: We found 2997 stringent peaks distributed on protein-coding genes, chiefly located in the promoter and the intron on VDRE DR3 sequences. However, the corresponding transcriptome data verified calcitriol-induced upregulation of only a small set of VDRTGs. The molecular network of 1541 calcitriol-responsive VDRTGs showed a significant relationship with leukocyte transendothelial migration, Fcγ receptor-mediated phagocytosis, and transcriptional regulation by VDR, suggesting a pivotal role of genome-wide VDRTGs in immune regulation. Conclusion: These results suggest the working hypothesis that persistent deficiency of vitamin D might perturb the complex network of VDRTGs in immune cells, being responsible for induction of an autoimmune response causative for MS.

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